The GI tract comprises the esophagus, the stomach, the small intestine, the large intestine, the colon, and the anal sphincter and is generally described as having a tract axis. Like other organs of the body, most notably the heart, these organs naturally undergo regular rhythmic contractions. In particular these contractions take the form of peristaltic contractions and are essential for the movement of food through each of the respective organs. Like the heart, these contractions are the result of regular rhythmic electrical depolarizations of the underlying tissue. With regards to the small intestine and large intestine, normal electrical depolarizations (“slow waves”) typically occur at a rate of approximately 15 and 1 beats per minute (bpm) respectively. Similarly, in the stomach, normal slow waves typically occur at a rate approximately 3 bpm. Not all of these depolarizations, however, normally result in a contraction of the organ. Rather contractions occur upon the occurrence of a normal electrical depolarizations followed by a series of high frequency spike activity.
In some individuals, however, either the regular rhythmic peristaltic contractions do not occur or the regular rhythmic electrical depolarizations do not occur or both do not occur. In each of these situations the movement of food may be seriously inhibited or even disabled. Such a condition is often called “gastroparesis” when it its occurs in the stomach. Gastroparesis is a chronic gastric motility disorder in which there is delayed gastric emptying of solids or liquids or both. Symptoms of gastroparesis may range from early satiety and nausea in mild cases to chronic vomiting, dehydration, and nutritional compromise in severe cases. Similar motility disorders occur in the other organs of the GI tract, although by different names.
Diagnosis of gastroparesis is based on demonstration of delayed gastric emptying of a radiolabeled solid meal in the absence of mechanical obstruction. Gastroparesis may occur for a number of reasons. Approximately one third of patients with gastroparesis, however, have no identifiable underlying cause (often called idiopathic gastroparesis). Management of gastroparesis involves four areas: (1) prokinetic drugs, (2) antiemetic drugs, (3) nutritional support, and (4) surgical therapy (in a very small subset of patients.) Gastroparesis is often a chronic, relapsing condition; 80% of patients require maintenance antiemetic and prokinetic therapy and 20% require long-term nutritional supplementation. Other maladies such as tachygastria or bradygastria can also hinder coordinated muscular motor activity of the GI tract, possibly resulting in either stasis or nausea or vomiting or a combination thereof.
The undesired effect of these conditions is a reduced ability or complete failure to efficiently propel intestinal contents down the digestive tract. This results in malassimilation of liquid or food by the absorbing mucosa of the intestinal tract. If this condition is not corrected, malnutrition or even starvation may occur. Moreover nausea or vomiting or both may also occur. Whereas some of these disease states can be corrected by medication or by simple surgery, in most cases treatment with drugs is not adequately effective, and surgery often has intolerable physiologic effects on the body.
For many years, sensing of the peristaltic electrical wave and gastrointestinal stimulation at various sites on or in the GI tract wall of the digestive system or nerves associated therewith have been conducted to diagnose and treat these various conditions. The history and breadth of such sensing and GI tract stimulation is set forth in commonly assigned U.S. Pat. Nos. 5,507,289, 6,026,326, 6,104,965, 6,216,039, and in further U.S. Pat. Nos. 5,690,691 and 6,243,607, for example.
Electrical stimuli are applied from the neurostimulator implantable pulse generator (IPG) through leads and electrodes affixed at sites in the body of the patient or the GI tract wall that permit the electrical stimulus to produce a local contraction of a desired portion of the GI tract. The sites of the GI tract wall comprise the outermost serosa or sub-serosally in the inner, circumferential and longitudinal (and oblique in the case of the stomach) smooth muscle layers referred to as the “muscularis externa”. The smooth muscle is preferably comprised of innervated muscle tissue, and it is theorized that the smooth muscle is neurally electrically stimulated through the nerves associated with and innervating the muscle tissue in order to produce the contraction of the smooth muscle.
An implantable method and system for electrical stimulation of smooth muscle with intact local gastric nerves comprising a portion of the GI tract is disclosed in the '607 patent. The electrical stimulation of the smooth muscle effects local contractions at sites of a portion of the GI tract that are artificially propagated distally therethrough in order to facilitate or aid at least a partial emptying of such portion. This stimulation attempts to create a simulated system that reproduces the spatial and temporal organization of normal gastric electrical activity by creating and controlling local circumferential non-propagated contractions. In this simulated gastric pacing system, each local circumferential contraction is invoked by applying an electrical stimulus to the smooth muscle circumferentially about the portion of the GI tract in a plane substantially perpendicular to the longitudinal axis of the portion. The electrical stimulus is applied at a proximal location and at at least one distal location. The distal location is in axially spaced relationship relative to the proximal location. Further, the applied electrical stimulus is selected to be sufficient to stimulate the smooth muscle to produce the local circumferential contractions at the proximal and distal locations.
The Medtronic® Itrel III® Model 7425 IPG and pairs of the unipolar Model 4300 or Model 4301 or Model 4351 “single pass” leads available from MEDTRONIC, INC. have been implanted to provide stimulation to sites in the stomach wall to treat chronic nausea and vomiting associated with gastroparesis. The unipolar electrode of these leads comprises a length of exposed lead conductor and is of the type disclosed in commonly assigned U.S. Pat. Nos. 5,425,751, 5,718,392 and 5,861,014. The above-referenced '039 patent and the '014 patent disclose the Model 4300 lead sewn through the serosa laterally into the muscularis externa to dispose the stimulation/sense electrode therein. A large incision is necessary to access the site, and a needle is used to perforate the serosa and muscularis externa laterally without fully penetrating the wall and to draw the stimulation/sense electrode into the muscularis externa. A laparascopic approach can be taken, but it is difficult to maneuver the needle to effect the fixation of the stimulation/sense electrode at the site. It is suggested in the '039 patent that two or more electrodes of this type can be formed along the length of the lead body that would be sewn laterally through and disposed within the muscularis externa.
The stimulation/sense electrodes conventionally employed in such gastrointestinal stimulation systems are formed of bio-compatible material shaped to either bear against the serosa or penetrate sub-serosally into the muscularis externa and polished to present an impervious outer surface. It is also suggested in the above-referenced '014 patent that the exposed electrode(s) of the single pass lead can alternatively be formed of other biocompatible electrode materials, including porous, platinized structures and could feature various pharmaceutical agents. Suggested pharmaceutical agents include dexamethasone sodium phosphate or beclomethasone phosphate in order to minimize the inflammatory response of the tissue to the implanted lead.
The above-referenced, commonly assigned, '326 patent shows a pin electrode mounted to extend orthogonally from a planar surface of a plate, wherein the pin electrode has a sharpened tip and is pressed through the serosa. The plate abuts against the serosa to limit the depth of penetration of the pin electrode to its length and has suture holes through it enabling the plate to be sutured to the GI tract wall to prevent dislodgement.
A further gastrointestinal lead bearing a pin electrode extending axially from the distal end of the lead body is disclosed in U.S. Pat. No. 5,423,872. In one version, the pin electrode is formed with distal tip retention barbs 21 that are pressed into the gastrointestinal wall and maintained in position by a suture passed through a suture pad. In a further version, more distally disposed and retractable barbs 37 are deployed to stabilize the pin electrode. In this variation, the lead body is formed with coaxial conductors to provide a bipolar lead, whereby a ring-shaped electrode 33 surrounds the distally and axially extending, pin electrode 31.
Thus, certain of the stimulation/sense electrodes that have been employed or disclosed in the above-referenced gastrointestinal stimulation systems are affixed in place by sutures, requiring surgical exposure of the GI tract wall at the site sufficient to enable suturing. In the case of the lead disclosed in the '872 patent, prevention of axial movement and perforation of the GI tract wall at the site of attachment cannot be assured by the limited engagement of the necessarily short and minute fixation barbs with the serosa or sub-serosa tissue. More robust fixation mechanisms are needed to avoid migration of the stimulation/sense electrode resulting either in dislodgement or perforation of the GI tract wall.
The above-described gastrointestinal leads have either unipolar electrodes or bipolar or multi-polar electrodes. The bipolar electrodes are typically disposed in close proximity to one another upon a single lead body or head or as sets of bipolar electrodes spaced apart along an elongated ribbon-like support as shown in the above-referenced '326 patent. It is generally desired to place individual electrodes of a bipolar electrode pair at least about 1.0 cm apart.
There are cases where the patient's stomach anatomy may not accommodate a lead that has two electrodes spaced apart by 1.0 cm or more in an axial arrangement along a lead body as suggested in the '039 patent or spaced apart by 1.0 cm or more on an electrode head or elongated ribbon-like support. For example, some patients have a jejunostomy feeding tube inserted into the stomach for supplemental nutrition, which may interfere with electrode placement, particularly relatively large electrode heads or elongated ribbon-like supports. This feeding tube is sometimes placed in the antrum of the stomach in the same location where it is desired to place electrodes to gastric stimulation for treatment of symptoms of gastroparesis. It is difficult to place bipolar electrodes in such a restricted area, and, when possible, the spacing between the electrodes may not be optimal.
Other patients may have had a surgical intervention, e.g., partial gastric resection for ulcer disease. In such cases, the remaining stomach may not be sufficiently large to place a bi-polar, single pass electrode of the type suggested in the above-referenced '039 patent into the circular muscle layer. And, the available surface area of the stomach to mount an electrode head or ribbon-like support of the types described above may not be available to locate the stimulation and/or sensing electrodes optimally.
Current neurostimulator IPGs are capable of operating with either unipolar or bipolar leads through bipolar connector sockets of the IPG header. If unipolar GI tract electrodes are employed to achieve the desired spacing in the affected regions, their proximal connector pins are each connected to one of the (typically) two available bipolar connector sockets of the neurostimulator IPG. Thus, when unipolar leads are employed, they restrict the number of stimulation/sense electrodes that could be employed with the neurostimulator IPG.
In the field of cardiac stimulation, cardiac pacing leads having bipolar and unipolar pace/sense electrodes have long been used in conjunction with pacing system IPGs to conduct pacing pulses generated by the IPG to a site of the heart and cardiac signals from the site to the IPG. Pacing leads are typically provided with a passive fixation or an active fixation mechanism at the lead body distal end that is passively or actively engaged with cardiac tissue to anchor a distal tip electrode at a desired site in or on the heart. Passive fixation generally involves an atraumatic fixation lodging the distal electrode against the endocardium or within a coronary blood vessel. Positive or active fixation generally involves a more traumatic penetration of a fixation mechanism into the myocardium from an endocardial or epicardial surface, and the active fixation mechanism commonly comprises a distal pace/sense electrode. Typically, the active fixation mechanism comprises the single pace/sense electrode or one of the bipolar pace/sense electrodes, but can be separate and electrically isolated from the pace/sense electrodes.
Endocardial pacing leads having either active fixation or passive fixation mechanisms are implanted by a transvenous route into a heart chamber to locate the distal pace/sense electrode(s) at a selected site in the heart chamber where an active or passive fixation mechanism is deployed to maintain the pace/sense electrode affixed at the site. Endocardial active fixation pacing leads typically employ extendable and retractable helixes or hooks that are retracted during introduction and are extended distally from the lead body distal end at the site of attachment as shown, for example, in commonly assigned U.S. Pat. No. 5,837,006.
Epicardial pacing leads are implanted by exposure of the epicardium of the heart through a limited thoracotomy. The distal end of the epicardial lead formed with one or two pace/sense electrodes and an active fixation mechanism supported by an electrode head is affixed to the epicardium. Active fixation mechanisms of epicardial pacing leads typically comprise a tissue penetrating, self-affixing mechanism extending away from a support or base or plate of the electrode head. The fixation mechanism is forced into the myocardium typically employing an insertion tool engaging the electrode head until it is fully seated within the endocardium and the plate bears against the epicardium. The plate is typically formed with a tissue ingrowth encouraging fabric or lattice, whereby tissue ingrowth about the plate assists in chronic anchoring to the heart.
One such active fixation, unipolar, epicardial pacing lead comprises the MEDTRONIC® Model 6917 and succeeding lead models that are disclosed in commonly assigned U.S. Pat. No. 3,737,579. The active fixation mechanism comprises a rigid helix having a sharpened tip that is coupled with a lead conductor within the electrode head and a helix axis. The helix is mounted to the electrode head such that the helix axis extends orthogonally to the plate. The distal electrode comprises an uninsulated portion of the helix. A bipolar version of leads of this type is disclosed in commonly assigned U.S. Pat. No. 4,010,758 wherein an annular or ring-shaped electrode is formed on the plate surface around the helix and coupled to a second lead conductor within the electrode head. Other variations of such unipolar or bipolar epicardial screw-in leads include multiple coaxial and intertwined helixes or a helix axially surrounding a pin extending coaxially with the helix axis from the electrode head. Other variations of such epicardial screw-in leads include multiple co-axial and intertwined helixes or a helix axially surrounding a pin extending coaxially with the helix axis from the electrode head, e.g., those shown in U.S. Pat. Nos. 4,235,246 and 4,452,254 and in UK Patent No. 1,277,107.
During implantation, the lead body and electrode head are mounted to an elongated tool, and the sharpened tip of the helix is advanced through the incision to perforate the epicardium. The tool and lead are rotated to screw the helix in until the plate abuts the epicardium, and the electrode head is detached from the tool.
A further epicardial screw-in lead is disclosed in commonly assigned U.S. Pat. No. 4,357,946 wherein the helix is mounted to a gear mechanism within the electrode head. The helix can itself be rotated to screw into the myocardium without rotating or moving the electrode head by a rotation of a removable stylet extending through the length of the lead body and engaging the gear mechanism. Both unipolar and bipolar embodiments are disclosed.
A further active fixation, unipolar, epicardial lead comprises the MEDTRONIC® Model 6951 lead disclosed in commonly assigned U.S. Pat. Nos. 4,313,448 and 4,424,818. The active fixation mechanism comprises forward facing barbed electrode having the tip at a predetermined angle with relation to the shank of the stimulation/sense electrode and with respect to a flexible base pad or plate of the electrode head. The plate has a substantially centered hole and a plurality of outer holes for fibrous ingrowth, and the shank of the stimulation/sense electrode extends out through the substantially centered hole. The barbed electrode is pushed into the myocardial tissue to the point where the base pad engages against the epicardium thereby indicating full implantation within the myocardium. During implantation, a stiffening stylet is employed to stiffen the lead body and a forceps is employed to grasp the electrode head to push the barb into the myocardium. A still further cardiac lead employing multiple hooks and a fixation tool for retracting the hooks during implantation is disclosed in U.S. Pat. No. 4,177,818.
Typically, cardiac pacing leads have a unitary lead body extending between a single distal pace/sense electrode or pair of pace/sense electrodes and a proximal connector assembly. However, bifurcated cardiac lead bodies extending to separate distal pace/sense electrodes are disclosed in U.S. Pat. Nos. 3,333,045, 3,472,234, 3,866,615, 4,000,745, 5,328,442, and 5,489,294.
Such active fixation, cardiac pacing leads with or without a bifurcated lead body have not, to our knowledge, been employed in the field of gastrointestinal stimulation. The myocardium is formed of muscle layers that are typically thicker and stiffer when pressed against than the muscle layers of the organ walls of the GI tract. The organ walls of the GI tract, e.g. the stomach wall, are thinner and more compliant and less massive than the heart wall, so they are difficult to prevent from simply collapsing when pressed against. The serosa is not a tough membrane that an electrode can catch in like the epicardium. Also, the overall mass of the heart is much greater than the stomach. For these reasons, it can be difficult to get anything like a hook or screw-in helix to penetrate the outer serosa of the GI tract, not perforate all the way through the GI tract wall and to stay affixed chronically.